Although recent studies have shown that alcohols can affect the function of certain neuronal neurotransmitter receptors, further work is needed to determine the mechanisms involved in those effects. This project used electrophysiological techniques to investigate the effects of alcohol on neuronal neurotransmitter receptors and the mechanisms involved in those effects. In a study of alpha beta epsilon delta nicotinic acetylcholine (nACh) receptors, ethanol potentiated currents activated by low ACh concentrations in a concentration-dependent manner over the concentration range 10-150 mM. In a study of the inhibition of ATP-activated current by ethanol, the inhibition was not significantly altered by the extracellular preapplication of phorbol 12-myristate 13-acetate (PMA), staurosporin, or forskolin. In addition, the inhibition was not significantly affected by the intracellular application of 100 mM ethanol in the patch pipette. Inclusion of GTP-gamma-S or GDP-beta-S in the pipette solution also failed to reverse the inhibitory effect of ethanol. In a study of the relationship between the hydrophobicity of various alcohols and their potency for inhibition of NMDA-activated current and potentiation of GABA-activated current, the slopes of the plots of potency vs. hydrophobicity were found to differ greatly for the short chain, less hydrophobic, alcohols. In a study of the potentiation of GABA-A receptors by n-alcohols, the potency of alcohols for enhancing GABA-activated current was found to increase as the carbon chain-length increased up to 11-12 carbons, but maximally-attainable concentrations of alcohols with more than 12 carbon atoms did not enhance GABA-activated current. This cutoff differs from those previously reported for behavioral measures of alcohol intoxication. The observations suggest that electrophysiological techniques will be useful for determining the cellular mechanisms of alcohol action in the nervous system.